Nakamura Kenta, Baba Ryoko, Kokubu Keiji, Harada Masaru, Morimoto Hiroyuki
Third Department of Internal Medicine, University of Occupational and Environmental Health, 1-1, Iseigaoka, Yahatanishi, Kitakyushu, Fukuoka 807-8555, Japan.
Department of Anatomy, School of Medicine, University of Occupational and Environmental Health, 1-1, Iseigaoka, Yahatanishi, Kitakyushu, Fukuoka 807-8555, Japan.
Acta Histochem Cytochem. 2024 Dec 20;57(6):199-209. doi: 10.1267/ahc.24-00049. Epub 2024 Dec 17.
Inflammatory bowel disease is triggered by abnormalities in epithelial barrier function and immunological responses, although its pathogenesis is poorly understood. The dextran sodium sulphate (DSS)-induced colitis model has been used to examine inflammation in the colon. Damage to mucosa primality occurs in the large intestine and scarcely in the small intestine. To evaluate the effect on the ileum, we histologically analyzed the inflammatory and recovery phases in DSS model mice, and 40 kDa FITC-dextran was used to investigate barrier function. In the inflammatory phase, histological damage was insignificant. However, expanded crypts, hypertrophic goblet and Paneth cells, increased mucus production and secretion were observed. The cellular morphology was restored to that of the control in the recovery phase. According to hybridization and lectin histochemistry, the expression of intestinal stem cell markers, secretory cell differentiation factors, and glycosylation of secretory granules in Paneth cells differed in the DSS model. DSS-treatment did not influence the barrier function in the ileum, and FITC-dextran did not diffuse the paracellular pathway into the mucosa. However, cells incorporating FITC appeared even under normal conditions. The number of FITC-positive Paneth cells was lower in the DSS group than the control group. Our results showed morphological and functional alterations in ileal epithelial cells, especially secretory cells, in the DSS colitis model.
炎症性肠病是由上皮屏障功能和免疫反应异常引发的，尽管其发病机制尚不清楚。葡聚糖硫酸钠（DSS）诱导的结肠炎模型已被用于研究结肠炎症。大肠会出现黏膜原始性损伤，而小肠几乎不会出现。为了评估对回肠的影响，我们对DSS模型小鼠的炎症期和恢复期进行了组织学分析，并使用40 kDa异硫氰酸荧光素标记的葡聚糖（FITC-葡聚糖）来研究屏障功能。在炎症期，组织学损伤不明显。然而，观察到隐窝扩张、杯状细胞和潘氏细胞肥大、黏液产生和分泌增加。在恢复期，细胞形态恢复到对照状态。根据杂交和凝集素组织化学分析，DSS模型中肠干细胞标志物的表达、分泌细胞分化因子以及潘氏细胞中分泌颗粒的糖基化存在差异。DSS处理对回肠的屏障功能没有影响，FITC-葡聚糖也不会通过细胞旁途径扩散到黏膜中。然而，即使在正常条件下也会出现摄取FITC的细胞。DSS组中FITC阳性潘氏细胞的数量低于对照组。我们的结果显示，在DSS结肠炎模型中，回肠上皮细胞，尤其是分泌细胞，存在形态和功能改变。
